Canonically, LC3 lipidation has been associated with autophagy pathways but it becomes increasingly clear that this modification can also occur during autophagy‐unrelated processes. In this issue, Florey and colleagues find that the WD40 domain of ATG16L1 is dispensable for LC3 lipidation during starvation‐induced autophagy but required for its lipidation during several other membrane‐based processes that are different from autophagy. This finding opens the door for the analysis of the functions of LC3 lipidation in these pathways.

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Ligase complex component ATG16L1 is required for LC3 lipidation of double‐membrane autophagsomes and of single membranes during phagocytosis and influenza infection, but only single membrane lipidation depends on ATG16L1's C‐terminal WD40 domain.

Synopsis

Ligase complex component ATG16L1 is required for LC3 lipidation of double‐membrane autophagsomes and of single membranes during phagocytosis and influenza infection, but only single membrane lipidation depends on ATG16L1's C‐terminal WD40 domain.

ATG16L1 recruitment to single‐membrane compartments during non‐canonical autophagy is dependent on the C‐terminal WD40 domain (CTD).

Modification of the ATG16L1 CTD offers a strategy to distinguish between canonical (macro)autophagy and non‐canonical autophagy processes.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Restriction of RAB7 GTPase activity and localization to specific endomembrane domains depends on the RAB7 effector retromer, thus equipping it with a function in autophagosome formation that is independent of its canonical endocytic recycling role.

Synopsis

Restriction of RAB7 GTPase activity and localization to specific endomembrane domains depends on the RAB7 effector retromer, thus equipping it with a function in autophagosome formation that is independent of its canonical endocytic recycling role.

This is an open access article under the terms of the Creative Commons Attribution 4.0 License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Nutrient removal from cancer cells is counterbalanced through p53‐dependent induction of pro‐survival lncRNA TRINGS and suppression of cell death signalling.

Synopsis

A screen for pathways by which p53 can play protective roles in tumor cell survival identifies the long non‐coding (lnc) RNA TRINGS (Tp53‐regulated inhibitor of necrosis under glucose starvation) as pro‐survival factor in cancer cells under nutrient stress, shedding light on tumorigenic roles of p53.

The p53‐dependent lncRNA TRINGS is expressed in human cancer cells upon glucose starvation.

p53 binding to the TRINGS promoter and transcriptional activity are required for TRINGS expression.

Necroptosis is a programmed form of inflammatory cell death involved in various pathologies, such as viral infections. In two new papers published in The EMBO Journal and EMBO Reports, Z‐DNA binding protein 1 (ZBP1) is now shown to sense RNAs during viral infection or after caspase inhibition and activate necroptosis. This may suggest that Z‐RNAs are molecular patterns for activation of necroptosis.